Lung volume reduction for emphysema using one-way endobronchial valves: An Australian cohort.

Emphysema can be associated with gas trapping and hyperinflation, which negatively impacts on quality of life, life expectancy, and functional capacity. Lung volume reduction (LVR) surgery can reduce gas trapping and improve mortality in select patients but carries a high risk of major complications. Bronchoscopic techniques for LVR using one-way endobronchial valves (EBV) have become an established efficacious alternative to surgery. A bi-center retrospective cohort study was conducted on patients with severe emphysema who underwent endoscopic lung volume reduction (ELVR) using Pulmonx Zephyr EBVs. Symptomatic patients with gas-trapping and hyperinflation on lung function testing were selected. Target-lobe selection was based on quantitative imaging analysis and ventilation-perfusion scintigraphy. Successful procedures were determined from clinical review, imaging and follow-up testing. Thirty-nine patients underwent ELVR. Mean pre-procedure forced expiratory volume in 1 second (FEV1) was 0.75 L, residual volume (RV) was 225% predicted and total lung capacity was 129% predicted. Most common treated-lobe was left upper lobe. Post-procedure pneumothorax occurred in 36.5% of patients with 73% requiring intercostal catheter insertion for drainage. Mean FEV1 improvement was +140 mL and 57% of patients achieved minimal clinical important difference FEV1 increase of ≥12%. Maximal mean RV change was -1010 mL with 69% of patients achieving minimal clinical important difference RV decrease of ≥350 mL. Clinician-determined success of ELVR was 78%. Procedure-related mortality was absent. LVR using EBVs is safe and can lead to significant improvements in lung function, particularly reduction of gas trapping and hyperinflation. Occurrence of pneumothorax post-procedure is a complication that must be monitored for and managed appropriately.

Effect of hyperhomocysteinemia on a murine model of smoke-induced pulmonary emphysema.

Hyperhomocysteinemia was reported to enhance endoplasmic reticulum (ER) stress and subsequent apoptosis in several cells. However, the precise mechanisms of smoking susceptibility associated with hyperhomocysteinemia has not been fully elucidated. This study included 7- to 9-week-old C57BL6 male mice induced with hyperhomocysteinemia and were exposed to cigarette smoke (CS). A549 cells (human alveolar epithelial cell line) were cultured with homocysteine and were exposed to cigarette smoke extract (CSE) to observe cell viability and expression of proteins related to the ER stress. After 6 months of CS exposure, pulmonary emphysema was more severely induced in the group under the condition of hyperhomocysteinemia compared to that in the control group. The apoptotic A549 cells increased as homocysteine concentration increased and that was enhanced by CSE. Protein expression levels of ER stress markers were significantly increased after simultaneous stimulation. Notably, vitamin B12 and folate supplementation improved ER stress after simultaneous stimulation of A549 cells. In this study, we showed that hyperhomocysteinemia exacerbates CS exposure-induced emphysema in mice, suggesting that hyperhomocysteinemia and CS stimulation enhance ER stress and subsequent induced apoptosis in alveolar epithelial cells. It was suggested that there is a synergistic effect between homocysteine and CS.

Emphysematous gastritis after metastatic malignant melanoma: a radiological surprise.

Malignant melanoma is cancer of the skin which commonly metastasises to the stomach. There have been no reported cases of emphysematous gastritis secondary to metastasis of malignant melanomas, to date. However, a 61-year-old woman with metastatic malignant melanoma of the left great toe presented to us with symptoms of severe left hypochondrium pain associated with high-grade fever, gross abdominal distension and recurrent vomiting. Two months earlier, metastasis was observed to have spread to the stomach and inguinal lymph nodes. At this stage, the patient opted for traditional medication instead of definitive surgery and chemotherapy. Radiological imaging revealed an emphysematous change to the stomach which was radiologically consistent with gastric malignant melanoma. Unfortunately, the patient succumbed to this rare condition.

Branch-like gas in a commercial diver's liver: a case report.

We report the case of a 42-year-old commercial diver who presented with palpitations, arthralgia, tachypnea and vomiting after three hours of repetitive dives to 25-30 meters below sea level (msw). He was diagnosed with severe decompression sickness (Type II DCS) based on his dive history, his abrupt ascent to the surface within minutes, and systemic symptoms with mild hypovolemic shock. Besides remarkable cutis marmorata on the torso, the patient was also found positive for diffuse branch-like pneumatosis in the liver, mesentery and intestines on an abdominal computed tomography (CT). His vitals were relatively stable, with a soft distended abdomen and mild tenderness over the right upper quadrant. He was treated with hyperbaric oxygen (HBO2) treatment in addition to essential crystalloid resuscitation. The abdominal pneumatosis resolved completely after two HBO2 sessions. Post-diving intra-abdominal pneumatosis is a rare complication of DCS. In our case it was difficult for dive doctors to diagnose promptly because an emergency abdominal CT was not a routine for potential DCS cases. We propose that a contrast-enhanced abdominal CT, which usually involves a intravenous injection of imaging agent, should be considered in emergency management of these patients, especially when they present with gastrointestinal symptoms.

Effect of Iron Deficiency on a Murine Model of Smoke-induced Emphysema.

Smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Smoking susceptibility is important for the onset and development of COPD. We previously reported an association between serum iron concentrations and pulmonary function in male smokers. However, the mechanism governing smoking susceptibility in relation to iron deficiency is unclear; this study aimed to elucidate this mechanism. C57BL/6 male mice were fed an iron-deficient or normal diet and then exposed to cigarette smoke. BAL, histological analysis, and pulmonary function tests were performed after cigarette smoke exposure. Human alveolar type II epithelial A549 cells were treated with an iron chelator. Subsequently, A549 cells were exposed to cigarette smoke extract. In mice exposed to cigarette smoke for 2 weeks, the concentration of alveolar macrophages in the BAL fluid recovered from iron-deficient mice was significantly higher than that in normal diet mice. IL-6 and MCP-1 (monocyte chemotactic protein 1) concentrations in the BAL fluid increased significantly from baseline in iron-deficient mice, but not in normal diet mice. In mice exposed to cigarette smoke for 8 weeks, the pathological mean linear intercepts, physiological total lung capacity, and functional residual capacity in the lungs of iron-deficient mice were significantly greater than in normal diet mice. Phosphorylation of NF-κB was enhanced in the lungs of iron-deficient mice exposed to cigarette smoke and in the iron-chelating A549 cells exposed to cigarette smoke extract. Iron deficiency exaggerated cigarette smoke-induced pulmonary inflammation, suggesting that it may accelerate COPD development.

Evaluation of bronchoscopic lung volume reduction coil treatment results in patients with severe emphysema.

INTRODUCTION: Bronchoscopic lung volume reduction coil (BLVR-C) implantation is an alternative therapeutic approach that can be applied together with medical treatment for patients with severe emphysema. BLVR-C is both easier and safer in terms of complications than volume reduction surgery. This study aimed to evaluate medium-term outcomes following BLVR-C treatment. METHODS: Forty patients who underwent BLVR-C between September 2013 and March 2014 were reviewed retrospectively. We compared changes between the baseline and 6-month post-procedural results with respect to pulmonary function tests, a 6-min walk test (6MWT), chronic obstructive pulmonary disease (COPD) assessment test (CAT), St. George's Respiratory Questionnaire (SGRQ), and pulmonary artery pressure (PAP) and arterial blood gas analyses. Secondary outcomes included procedure-related and follow-up complications. RESULTS: An average of 9.5 (range: 5-11) coils were placed per lung in an average procedural duration of 20.8 ± 7.0 min (range: 9-45) min. Six months after BLVR-C treatment, significant improvements were observed in patients' pulmonary function tests and quality of life. Changes were observed in the forced exhalation volume in 1 s (+150 mL), residual volume (-14.5%), 6MWT (+48 m), SGRQ (-10.5) and CAT Score (-7.5). Changes in the PAP and partial pressure of carbon dioxide values were not significant, and pneumothorax did not occur. In a 6-month follow-up, 11 cases of COPD exacerbation (41.4%), 7 cases of pneumonia (16.9%) and 1 death (2%) occurred. Treatment in 1 case was postponed because of hypotension and bradycardia during the process. CONCLUSION: BLVR-C treatment appears to be effective over the medium-term and safe for patients with severe emphysema.

Agonistic induction of PPARγ reverses cigarette smoke-induced emphysema.

The development of emphysema in humans and mice exposed to cigarette smoke is promoted by activation of an adaptive immune response. Lung myeloid dendritic cells (mDCs) derived from cigarette smokers activate autoreactive Th1 and Th17 cells. mDC-dependent activation of T cell subsets requires expression of the SPP1 gene, which encodes osteopontin (OPN), a pleiotropic cytokine implicated in autoimmune responses. The upstream molecular events that promote SPP1 expression and activate mDCs in response to smoke remain unknown. Here, we show that peroxisome proliferator-activated receptor γ (PPARG/Pparg) expression was downregulated in mDCs of smokers with emphysema and mice exposed to chronic smoke. Conditional knockout of PPARγ in APCs using Cd11c-Cre Pparg(flox/flox) mice led to spontaneous lung inflammation and emphysema that resembled the phenotype of smoke-exposed mice. The inflammatory phenotype of Cd11c-Cre Pparg(flox/flox) mice required OPN, suggesting an antiinflammatory mechanism in which PPARγ negatively regulates Spp1 expression in the lung. A 2-month treatment with a PPARγ agonist reversed emphysema in WT mice despite continual smoke exposure. Furthermore, endogenous PPARγ agonists were reduced in the plasma of smokers with emphysema. These findings reveal a proinflammatory pathway, in which reduced PPARγ activity promotes emphysema, and suggest that targeting this pathway in smokers could prevent and reverse emphysema.

Induction of lung emphysema is prevented by L-arginine-threonine-arginine.

In patients with chronic obstructive pulmonary disease (COPD), an inflammatory process is ongoing in the lungs, with concomitant damage of the alveolar structures and loss of airway function. In this inflammatory process, extracellular matrix degradation is observed. During this lung matrix degradation, small peptide fragments consisting of proline and glycine repeats generated from collagen fibers are liberated from the matrix by matrix metalloproteinases. Chemotactic activities of these collagen-derived peptides such as N-acetyl-proline-glycine-proline (PGP) via CXCR1 and CXCR2 have been reported. We show here that PGP induces neutrophil migration in vivo, which is dose dependent. Moreover, PGP is involved in the development of emphysema-like changes in the airways. The complementary peptide, L-arginine-threonine-arginine (RTR), has been shown to bind to PGP sequences and inhibit neutrophil infiltration. We show that RTR impedes both PGP- and interleukin-8-induced chemotaxis in vitro. In vivo, RTR prevents both migration and activation of neutrophils induced by PGP. Furthermore, RTR completely inhibits PGP-induced lung emphysema, assessed by changes in alveolar enlargement and right ventricular hypertrophy. In conclusion, these data indicate that collagen breakdown products, especially PGP, are important in the pathogenesis of COPD and that PGP antagonism via RTR ameliorates lung emphysema.

Tomato juice prevents senescence-accelerated mouse P1 strain from developing emphysema induced by chronic exposure to tobacco smoke.

The senescence-accelerated mouse (SAM) is a naturally occurring animal model for accelerated aging after normal development and maturation. SAMP1 strain was reported to show age-related structural and functional changes in lung and to be a murine model of senile lung. We postulated that aging of lung is an important intrinsic process for development of emphysema and even in a short period of tobacco smoke exposure may be able to generate emphysema. At age 12 wk, SAMP1 inhaled air or 1.5% tobacco smoke (total particulate matter 23.9 mg/m3) through the nose for 30 min/day, 5 days/wk, and for 8 wk. The mean linear intercepts (MLI) and destructive index (DI) of lung were significantly increased [air vs. smoke (means+/-SE); MLI, 68.76+/-0.69 vs. 75.34+/-1.70 microm, P<0.05 and DI, 8.61+/-0.38 vs. 16.18+/-1.54%, P<0.05], whereas no significant changes were observed in SAMR1, control mice that show normal aging. In contrast, smoke-induced emphysema was completely prevented by concomitant ingestion of lycopene given as tomato juice [MLI: smoke with/without lycopene (mean+/-SE), 62.87+/-0.8 vs. 66.90+/-1.33 microm, P<0.05]. Smoke exposure increased apoptosis and active caspase-3 of airway and alveolar septal cells and reduced VEGF in lung tissues, but tomato juice ingestion significantly reduced apoptosis and increased tissue VEGF level. We conclude that SAMP1 is a useful model for tobacco smoke-induced emphysema and a valuable tool to explore both pathophysiological mechanisms and the effect of therapeutic intervention on smoke-induced emphysema.

Bilateral emphysematous pyelonephritis resolving to medical therapy.

We describe a case of bilateral emphysematous pyelonephritis, in a diabetic female, that responded to medical therapy alone. Her complete improvement is documented radiologically. Emphysematous pyelonephritis, as a cause of serious infection in diabetic patients, is briefly reviewed.

Iatrogenic retropharyngeal emphysema with impending airway obstruction.

The causes, diagnosis, sequelae, and treatment of interstitial emphysema of the face, neck, and thorax have been previously described in the medical and dental literature and are reviewed here. We present a unique case of a patient who, following dental amalgam restoration, developed severe retropharyngeal emphysema with impending airway obstruction, cervicofacial subcutaneous emphysema, and pneumomediastinum. Management consisted of urgent tracheotomy, broad-spectrum prophylactic antibiotic coverage, close observation, and reassurance. The likely mechanisms of precipitation and extension of the emphysema in this patient are discussed.

Pneumoperitoneum, omental emphysema and intramural barium perforation following double contrast barium enema.

Perforation above the peritoneal reflection is a rare complication of a barium enema. We describe a case in which perforation in the transverse colon during a double contrast study resulted in intramural extravasation of barium, pneumoperitoneum and omental emphysema.

Diagnosis and treatment of retroperitoneal perforation complicating the double-contrast barium-enema examination.

A case of retroperitoneal air caused by rectal perforation during a double-contrast barium-enema examination is reported. In 9 similar reported cases, radiographic signs included perirectal, mediastinal, and cervical emphysema. Because of the frequent absence of clinical signs, radiographic recognition may be crucial for prompt management. Reported experience suggests that asymptomatic patients with these radiographic findings may be managed with hospitalization and close observation rather than immediate laparotomy.